Normal Breathing
For air to flow into the lungs, the gas pressure in the gas exchanging units, the alveoli, must be lowered to below that at the airway opening. At the end of expiration, when there is no airflow, the pressure in the alveoli is the same as atmospheric. To get air into the lungs, the pressure in the chest surrounding the lungs, intrathoracic pressure, must be lowered to below atmospheric. This is accomplished by contraction of the inspiratory muscles which enlarges the thorax and further lowers the intrathoracic pressure (the intrathoracic or pleural pressure is already slightly sub-atmospheric due to the elastic recoil of the lungs and chest wall). The lower intrathoracic pressure expands the alveoli, thus lowering the intra-alveolar gas pressure below atmospheric so that air flows into the lungs.
Taking a breath requires that the inspiratory muscles generate sufficient force to overcome the elastic recoil of the lungs and chest wall, frictional lung and chest wall tissue resistance, and the frictional resistance to airflow through the airways. At the end of an inspiration, the potential energy stored in the tissues of the lungs and chest wall is available to allow rapid passive exhalation when the inspiratory muscles cease contraction and the distending force disappears. All intrathoracic structures, including the heart and great veins, are subjected to the pressures generated by breathing, either due to spontaneous or mechanical ventilation.
Measurement of Central Venous Pressure
During inspiration the central venous pressure (CVP) decreases, aiding the return of blood to the heart. Changes in pleural or intrathoracic pressure due to respiration are reflected by and can be timed to changes in central venous pressure. When recumbent, the internal and external jugular veins are open and provide the primary cerebral venous and superficial forehead venous return. The communication between the superior vena cava and the veins of the head allows intrathoracic pressure changes to be reflected by the superficial veins of the head. In a sense, the forehead veins offer a direct fluid filled catheter into the thoracic cavity, and when the correct compressive force is applied against the skull, respiratory effort linked venous pressure changes can be accurately measured. When upright, the jugular veins tend to collapse and venous outflow is distributed to the vertebral venous plexus for return.
The head is relatively highly vascularized and when a person is recumbent so that the vertical position of the optical sensors is close to that of the right atrium, venous pressure is about the same as the pressure in the superior vena cava. Thus the head and neck provide a number of sites that can be used for indirect measurement of CVP. These sites include but are not limited to the forehead (frontal, superficial temporal, supra-orbital, and angular veins), cheek (transverses facial vein), nose (nasal arch and supra labial) or neck (posterior external plexus). Indirect measurement of CVP may also be performed from any site on the body that has sufficient venous flow. For example, veins on the dorsum of the hand or cephalic or balisic veins of the arm may provide alternate sites for monitoring changes in CVP.
The most common method of monitoring CVP is by insertion of a central venous catheter, but this is not optimal for routine monitoring. Complications of central venous catheter placement include carotid artery puncture, pneumothorax, cardiac tamponade, arrythmias, and major air embolism. Infection is the major complication of prolonged central catheters. CVP can be obtained with transducers and electronic monitors, with a simple water manometer or, during clinical examination, by measuring jugular venous distension. Thus, any measure of CVP that can be performed either from the surface of the skin or non-invasively would be beneficial.